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Study indicates vitamin D deficiency can lead to dementia
New research suggests low levels of vitamin D are associated with lower brain volumes, and an increased risk of dementia and potentially stroke.
Genetic research out of the University of South Australia (UniSA) has found a direct link between dementia and a lack of vitamin D.
The study, published in The American Journal of Clinical Nutrition, investigated the association between vitamin D, neuroimaging features, and the risk of dementia and stroke, finding that:
- low levels of vitamin D were associated with lower brain volumes and an increased risk of dementia and stroke
- genetic analyses supported a causal effect of vitamin D deficiency and dementia
- in some populations as much as 17% of dementia cases might be prevented by increasing people to normal levels of vitamin D (50 nmol/L).
About 487,500 Australians live with dementia, which is the
leading cause of death among women and the
second leading cause of death overall.
Supported by the National Health and Medical Research Council, the genetic study analysed data from 294,514 participants from the UK Biobank, examining the impact of low levels of vitamin D (25 nmol/L) and the risk of dementia and stroke.
Senior investigator and Director of UniSA’s Australian Centre for Precision Health, Professor Elina Hyppönen, says the findings are important for the prevention of dementia and appreciating the need to abolish vitamin D deficiency.
‘Vitamin D is a hormone precursor that is increasingly recognised for widespread effects, including on brain health, but until now it has been very difficult to examine what would happen if we were able to prevent vitamin D deficiency,’ she said.
‘Our study is the first to examine the effect of very low levels of vitamin D on the risks of dementia and stroke, using robust genetic analyses among a large population.
‘In some contexts, where vitamin D deficiency is relatively common, our findings have important implications for dementia risks. Indeed, in this UK population we observed that up to 17% of dementia cases might have been avoided by boosting vitamin D levels to be within a normal range.’
Nonlinear Mendelian randomisation (MR) – a method of using measured variation in genes to examine the causal effect of a modifiable exposure on disease – were used to test for underlying causality for neuroimaging outcomes, dementia, and stroke.
While the MR results suggested no clear association with stroke, it confirmed a causal relation with dementia risk, which the researchers believe provides an ‘important opportunity for prevention’.
Likewise, the finding that the strongest effects on dementia risk were seen for those with the lowest vitamin D concentrations (<25 nmol/L) was consistent in both observational and MR analyses.
For Professor Hyppönen, the findings are significant given the high prevalence of dementia around the world.
‘Dementia is a progressive and debilitating disease that can devastate individuals and families alike,’ she said.
‘If we’re able to change this reality through ensuring that none of us is severely vitamin D deficient, it would also have further benefits and we could change the health and wellbeing for thousands.
‘Most of us are likely to be ok, but for anyone who for whatever reason may not receive enough vitamin D from the sun, modifications to diet may not be enough, and supplementation may well be needed.’
The researchers believe that it is ‘biologically plausible’ that vitamin D could have a protective effect on brain health, suggesting three possible mechanisms
‘First, the presence of vitamin D receptors in the hypothalamus has suggested a neurosteroid function for active vitamin D, promoting the growth and maturation of neurons,’ they wrote.
‘Second, there may be vascular mechanisms as active vitamin D has been associated with reduced thrombosis and regulation of the renin–angiotensin system.
‘Third, replete concentrations of active vitamin D may act as a neuroprotectant through the suppression of excess inflammatory neurovascular damage caused by proinflammatory cytokines and attenuation of amyloid proteins, commonly observed in Alzheimer disease.’
Study limitations cited by the research team include an inability to rule out influences by residual confounding in their observational analyses, while the UK Biobank was labelled ‘vulnerable to healthy volunteer bias’ as the baseline population was mostly less deprived, had intermediate to high education, and had a normal to overweight BMI (50).
Meanwhile, as the MR analyses were restricted to participants from white British ancestry, these findings may not be generalisable to other populations.
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